Both 25-Hydroxyvitamin-D3 and 1,25-Dihydroxyvitamin-D3 Reduces Inflammatory Response in Human Periodontal Ligament Cells

Andrukhov, Oleh; Andrukhova, Olena; Hulan, Ulamnemekh; Tang, Yan; Bantleon, Hans-Peter; Rausch‐Fan, Xiaohui

doi:10.1371/journal.pone.0090301

Cited by 63 publications

(96 citation statements)

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“…Recently, Andrukhov and colleagues reported that 1,25-dihydroxyvitamin D3 and 25-hydroxyvitamin D3 could inhibit IL-6, IL-8, and CCL2 productions from P. gingivalis-stimulated HPDLC [33]. We revealed calcitriol suppressed not only inflammatory cytokines but Th17 chemokine, Th1 chemokine, and matrix metalloproteinase production through JNK and NF-κB pathway inhibition.…”

Section: Discussionmentioning

confidence: 52%

Calcitriol Suppressed Inflammatory Reactions in IL-1β-Stimulated Human Periodontal Ligament Cells

Hosokawa

Shindo

et al. 2015

Inflammation

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Vitamin D has important roles on control of calcium and phosphate levels in the body. However, the role of vitamin D on the pathogenesis of periodontal disease is still uncertain. Therefore, we examined the effect of the hormonal form of vitamin D, calcitriol, on inflammatory responses of human periodontal ligament cells (HPDLC). We detected vitamin D receptor expression in non-stimulated HPDLC. Calcitriol inhibited interleukin (IL)-6, IL-8, CC chemokine ligand (CCL) 20, CXC chemokine ligand (CXCL) 10, and matrix metalloproteinase (MMP)-3 release from IL-1β-stimulated HPDLC. Tissue inhibitor of metalloproteinase (TIMP)-1 production did not change by calcitriol. Moreover, we found c-jun N-terminal kinase (JNK) phosphorylation and IκB-α degradation in IL-1β-stimulated HPDLC were inhibited by calcitriol, and JNK and nuclear factor (NF)-κB inhibitors could decrease IL-6, IL-8, CCL20, CXCL10, and MMP-3 productions in IL-1β-treated HPDLC. These findings suggest that vitamin D could modulate inflammatory response in periodontal tissues.

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Section: Discussionmentioning

confidence: 52%

Calcitriol Suppressed Inflammatory Reactions in IL-1β-Stimulated Human Periodontal Ligament Cells

Hosokawa

Shindo

et al. 2015

Inflammation

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“…It can influence dendritic cell maturation and function, enhance the phagocytic and chemotactic function of monocytes and macrophages, and regulate T-and B-lymphocyte proliferation, differentiation, and cytokine secretion (18)(19)(20)(21)(22)(23)(24). In recent years, several studies have demonstrated that vitamin D can modulate inflammation via the regulation of cytokine production (21,25). Tang et al reported that vitamin D might potentially inhibit periodontal inflammation induced by Pg, partly by decreasing the cytokine expression in human periodontal ligament cells (26).…”

Section: Discussionmentioning

confidence: 99%

Effects of 1,25-dihydroxyvitamin D<sub>3</sub> on Macrophage Cytokine Secretion Stimulated by <i>Porphyromonas gingivalis</i>

Zhang

et al. 2016

Jpn J Infect Dis

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SUMMARY: Vitamin D is known to be closely associated with periodontitis; however, its exact mechanisms remain to be clarified. The present study aimed to investigate the influence of 1,25-dihydroxyvitamin D 3 (1,25(OH) 2 D 3 ) on Porphyromonas gingivalis (Pg)-stimulated cytokine production and the involved signaling pathways in macrophages. The main observation was that 1,25(OH) 2 D 3 inhibited Pg-induced interleukin (IL)-6 cytokine expression but up-regulated the expression of antiinflammatory cytokine IL-10. Further analyses showed that 1,25(OH) 2 D 3 decreased p38 mitogen-activated protein kinase (MAPK) and extracellular signal regulated kinase (ERK)1/2 phosphorylation. Inhibited phosphorylation of p38 MAPK and ERK1/2 was associated with decreased level of IL-6 expression, but was not related to increased level of IL-10 expression in macrophages stimulated with Pg. These results suggest that 1,25(OH) 2 D 3 might exert its anti-inflammatory effects on Pg-stimulated macrophages partly through its inhibitory effect on the p38 MAPK and ERK1/2 signaling pathway.

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“…Importantly, treatment with VDR siRNA abolishes the 1,25D3-evoked attenuation of proinflammatory cytokine/chemokine expression in human periodontal ligament fibroblasts stimulated with Porphyromonas gingivalis lipopolysaccharide, showing that 1,25D3 acts through VDR [38].…”

Section: 25d3 Differentially Attenuates Cytokine/chemokine Productimentioning

confidence: 94%

“…On the other hand, Andrukhov et al [38] report that 1,25D3 reduces the production of all three pro-inflammatory cytokines IL-6, IL-8 and CCL2…”

Section: 25d3 Differentially Attenuates Cytokine/chemokine Productimentioning

confidence: 99%

“…Porphyromonas gingivalis and lipopolysaccharide-induced IL-8 and CCL2 chemokine mRNA expression and protein production, while it has no effect on IL-6 in primary human periodontal ligament cells [37,38]. On the other hand, Andrukhov et al [38] report that 1,25D3 reduces the production of all three pro-inflammatory cytokines IL-6, IL-8 and CCL2…”

Section: 25d3 Differentially Attenuates Cytokine/chemokine Productimentioning

confidence: 99%

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Vitamin D3 modulates the innate immune response through regulation of the hCAP-18/LL-37 gene expression and cytokine production

2015

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The steroid hormone metabolite of vitamin D 3 , 1α,25-dihydroxyvitamin D 3 (1,25D3), promotes osteogenic activity and regulates calcium and phosphate metabolism, which are actions regarded as classical vitamin D-regulated functions. Besides its role in these processes, 1,25D3 also seems implicated in the host defense against microbial/proinflammatory attacks. Low serum levels of vitamin D 3 (vitamin D deficiency) are associated with osteoporosis and increased risk of fractures but also inflammatory diseases and their disease progression, presumably via mechanisms associated with 1,25D3-evoked modulation of the innate immune system. 1,25D3 has been reported to modulate many inflammatory responses, suggesting that it regulates multiple transcriptional targets within the inflammatory system. Experimental studies in various experimental systems show that 1,25D3 differentially regulates the production of pro-inflammatory cytokines and chemokines depending on cell type. Importantly, many reports show that 1,25D3 up-regulates expression of the human antimicrobial peptide hCAP-18/LL-37 gene. The hCAP-18/LL-37 gene seems indeed to be an important transcriptional target for 1,25D3. However, only weak evidence is presented showing that 1,25D3 consistently increases the amount of biologically active LL-37 peptide.In the present review, we discuss 1,25D3-induced down-regulation of cytokine/chemokine production and stimulation of hCAP-18/LL-37 gene expression which represent two very important pathways for 1,25D3-evoked regulation of the innate immune response.

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Both 25-Hydroxyvitamin-D3 and 1,25-Dihydroxyvitamin-D3 Reduces Inflammatory Response in Human Periodontal Ligament Cells

Cited by 63 publications

References 50 publications

Calcitriol Suppressed Inflammatory Reactions in IL-1β-Stimulated Human Periodontal Ligament Cells

Calcitriol Suppressed Inflammatory Reactions in IL-1β-Stimulated Human Periodontal Ligament Cells

Effects of 1,25-dihydroxyvitamin D<sub>3</sub> on Macrophage Cytokine Secretion Stimulated by <i>Porphyromonas gingivalis</i>

Vitamin D3 modulates the innate immune response through regulation of the hCAP-18/LL-37 gene expression and cytokine production

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